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Gastrointestinal toxicity induced by microcystins

Gastrointestinal toxicity induced by microcystins

作     者:Jin-Xia Wu Hui Huang Lei Yang Xiao-Feng Zhang Shen-Shen Zhang Hao-Hao Liu Yue-Qin Wang Le Yuan Xue-Min Cheng Dong-Gang Zhuang Hui-Zhen Zhang 

作者机构:Department of Environmental Hygiene College of Public Health Zhengzhou University Department of Nutriology College of Public Health Zhengzhou University 

出 版 物:《World Journal of Clinical Cases》 (世界临床病例杂志)

年 卷 期:2018年第6卷第10期

页      面:344-354页

核心收录:

学科分类:10[医学] 

基  金:Supported by Henan Natural Science Foundation,No.162300410267 the National Nature Science Foundation of China,Nos.81773384 and 81472948 

主  题:Immunotoxicity Gastrointestinal toxicity Intestine Depuration Oxidative stress Microcystins 

摘      要:Microcystins(MCs) are produced by certain bloomforming cyanobacteria that can induce toxicity in various organs, including renal toxicity, reproductive toxicity, cardiotoxicity, and immunosuppressive effects. It has been a significant global environmental issue due to its harm to the aquatic environment and human health. Numerous investigators have demonstrated that MC exposure can induce a widespread epidemic of enterogastritis with symptoms similar to food poisoning in areas close to lakes. Both in vivo and in vitro studies have provided evidence of positive associations between MC exposure and gastrointestinal toxicity. The toxicity of MCs on the gastrointestinal tract is multidimensional. MCs can affect gastrointestinal barrier function and shift the structure of gut microbiota in different gut regions. Furthermore, MCs can inhibit the secretion of gastrointestinal digestive enzymes and the release of inflammatory cytokines, which affects the expression of immune-related genes in the intestine. The damage of the intestine is closely correlated to MC exposure because the intestine is the main site for the digestion and absorption of nutrients. The damage to the gastrointestinal tract due to MCs was summarized from different aspects, which can be used as a foundation for further exploration of molecular damage mechanisms.

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